CCL2 and endothelial dysfunction: Proinflammatory stimuli, including oxLDL, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β), IL-6, and monocyte chemoattractant protein-1 (MCP-1), increase the production of ROS and induce endothelial dysfunction through a variety of signaling pathways involved in activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways [45,47,48,49].